Atrial fibrillation

Less is more in atrial fibrillation stroke prevention — please, drop the aspirin

A recent study in the Journal of the American College of Cardiology shed more light on the commonly used drug combination of aspirin and a vitamin-K antagonist (such as warfarin).  It was a small registry study from one region of France but I believe it offered confirmatory evidence against this dangerous practice.

Investigators followed patients with stable coronary artery disease (no recent events) for 2 years to assess the incidence and outcomes of major bleeding episodes. They found that overall rates of major bleeding were less than 1%, but those patients on the combination of aspirin and an anticoagulant drug were almost five times more likely to suffer major bleeds. In fact, the combination was the major predictor of bleeding–more than two-fold greater than diabetes.

The reason why I point you to this study is that the practice of combining clot-preventing drugs in patients with AF is one I see so frequently. And I’m not an outlier, registry studies suggest up to 40% of AF patients are taking the combination.

This is a bad idea. It needs to stop.

Screen Shot 2014-09-30 at 7.07.47 AMThe French study aligns well with prior evidence on combining drugs. In March of 2013, I published this review of the existing data on My conclusion was that, in the great majority of patients, there was no evidence for added stroke protection but there was a compelling signal of higher bleeding. Only three subgroups of patients fell out of this general statement. The ratio of benefit to harm may be positive in patients with AF and mechanical heart valves, AF and recent stents or AF and recent acute coronary syndrome. That’s it.

The vast majority of AF patients taking this combination likely should not be.

I do a lot of deprescribing these days. Aspirin, when used in AF patients who are on anticoagulant drugs, is perhaps the most common drug I deprescribe.

Look at the data yourself and see if you come to a different conclusion. My article on has references.


8 replies on “Less is more in atrial fibrillation stroke prevention — please, drop the aspirin”

Does this apply to simvastatin and the like? John and I are both taking these prescriptions and the low dose aspirin daily. I notice I bruise easily at the slightest bump and have an ugly black and blue mark just from bumping into an elevator door a few weeks ago!

Nicely stated John! For those with interest in the subject – your March, 2013 column on the “dangerous cocktail of ASA & anticoagulants” is worth a reread. You nicely make the point that ONLY those with specific indication should receive both ASA and anticoagulants due to significant increased bleeding risk without associated benefit in most patients who are taking the combination.

Dr. John:

I’m glad you brought this up. I have a few questions.

If a person, a middle aged male, was prescribed low dose aspirin prior to a diagnosis of afib, would the anticoagulant prescribed for afib protect against plaque related strokes and MIs as well as an antiplatelet? (I know there are some studies that indicate that aspirin is more effective in preventing second MIs rather than 1st MIs, and I guess the same for stroke. But assume the aspirin was properly prescribed. Would the anticoagulant provide the same protection?

The study addressed vitamin K antagonists like warfarin, not the NOACs. Do you see a difference? If so, which NOACs would be safer with antiplatelets (if any)?

These questions may seem hypothetical, but since both afib and heart disease are most frequent in those in their sixties and later, this situation must come up a lot. That brings me to a few more questions.

Since virtually all males seventy and older have some coronary calcium (indicating some plaque is present) according to the companies that administer the tests, would you say that virtually all males seventy and older have coronary artery disease?

Is there any value in distinguishing coronary ARTERY disease from coronary HEART disease? I see some medical sites saying they are different based on where the calcium or plaque is located, and some sites that say the two are synonymous. I guess the easy answer is- if you have plaque in your arteries, you likely have it in the heart itself… but maybe it isn’t true.

As patients, we look at both structural and electrical aspects of our heart health. We can’t ignore either one, and we certainly don’t want the treatment of one to negatively affect treatment of the other.


1) Yes, anticoagulant drugs do seem to offer similar “anti-thrombotic” secondary protection. See this old NEJM article on warfarin, asa or both after MI.

2) The risk of the combination of two clot-inhibiting drugs does seem to pertain to the NOAC agents as well, though there is less data. See the hyprlinked article. I have a couple of paragraphs there on the matter.

3) The third one is a tougher question– on aging and coronary calcium and whether we say coronary heart disease. I think the semantics aren’t that important. The best way to not get coronary calcium, or AF for that matter, is to to die at a young age. Calcification of things in the body is part of the aging process, which can’t be stopped, but can be slowed. How to slow it? Well, you know…eat well, sleep well, move a lot, and not worry too much about coronary calcium (because there are bike rides to have and good novels to read, etc).

Your last paragraph highlights a point I make to patients nearly every day. Namely, the heart’s rhythm, or lack of rhythm, can be more than just a primary disease (or cause.) It’s also a secondary manifestation on how we are doing as a whole person (or an effect). As in, when we are well overall, our hearts are too. > Because it’s all connected.

Agree, but would point out that for some indications, conclusions favoring the use (or additional use) of aspirin over-look the fact that INRs were intentionally low (as in some of the big post MI/ACS studies such as CARS and CHAMP) or unintentionally had a large % of INRs below target (as in prosthetic valve studies with > 40% INR below target range) and even in secondary prevention of vascular disease-related stroke, when conclusion was that ASA was as good as or better than warfarin, the stroke rate when the INR was in range was about 40% lower with warfarin than with ASA. Some counter-balancing info is new stronger data supporting anti-cancer effect with long-term aspirin; but there is also conflicting data as to whether warfarin may have anti-cancer effects.

I stopped paying attention to these studies that contradict each other, particularly when they are observational. I would think there would be a difference between those who have an afib attack once a year versus 30 times a month. Both are paroxysmal. But statements like the following make me question these articles:

“Dr Vanassche said: “Other studies have shown that patients with permanent AF are often younger and at a lower risk of stroke compared to those with permanent AF…”

It can be a challenge to properly treat and prevent symptomatic illnesses related to heart disease, but an informed take on proper courses of action is much needed. Thanks for sharing.

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